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Journal Articles

Allorestricted T cells with specificity for the FMNL1-derived peptide PP2 have potent antitumor activity against hematologic and other malignancies

Ingrid G. Schuster, Dirk H. Busch, Elfriede Eppinger, Elisabeth Kremmer, Slavoljub Milosevic, Christine Hennard, Christina Kuttler, Joachim W. Ellwart, Bernhard Frankenberger, Elfriede Nößner, Christoph Salat, Christian Bogner, Arndt Borkhardt, Hans-Jochem Kolb, Angela M. Krackhardt

Blood (2007) 110 (8): 2931–2939.

https://doi.org/10.1182/blood-2006-11-058750

Published: 2007

Includes: Supplemental data

Journal Articles

Point mutations in the juxtamembrane domain of FLT3 define a new class of activating mutations in AML

Carola Reindl, Ksenia Bagrintseva, Sridhar Vempati, Susanne Schnittger, Joachim W. Ellwart, Katja Wenig, Karl-Peter Hopfner, Wolfgang Hiddemann, Karsten Spiekermann

Blood (2006) 107 (9): 3700–3707.

https://doi.org/10.1182/blood-2005-06-2596

Published: 2006

Journal Articles

Point Mutations Found in the Juxtamembrane Domain of FLT3 Define a New Class of Activating Mutations in AML.

Carola Reindl, Ksenia Bagrintseva, Susanne Schnittger, Joachim W. Ellwart, Katja Wenig, Karl-Peter Hopfner, Wolfgang Hiddemann, Karsten Spiekermann

Blood (2005) 106 (11): 4388.

https://doi.org/10.1182/blood.V106.11.4388.4388

Published: 2005

Journal Articles

FLT3-ITD-TKD dual mutants associated with AML confer resistance to FLT3 PTK inhibitors and cytotoxic agents by overexpression of Bcl-x(L)

Ksenia Bagrintseva, Stefanie Geisenhof, Ruth Kern, Sabine Eichenlaub, Carola Reindl, Joachim W. Ellwart, Wolfgang Hiddemann, Karsten Spiekermann

Blood (2005) 105 (9): 3679–3685.

https://doi.org/10.1182/blood-2004-06-2459

Published: 2005

Journal Articles

KIT exon 8 mutations associated with core-binding factor (CBF)–acute myeloid leukemia (AML) cause hyperactivation of the receptor in response to stem cell factor

Tobias M. Kohl, Susanne Schnittger, Joachim W. Ellwart, Wolfgang Hiddemann, Karsten Spiekermann

Blood (2005) 105 (8): 3319–3321.

https://doi.org/10.1182/blood-2004-06-2068

Published: 2005

Journal Articles

Mutations in the tyrosine kinase domain of FLT3 define a new molecular mechanism of acquired drug resistance to PTK inhibitors in FLT3-ITD–transformed hematopoietic cells

Ksenia Bagrintseva, Ruth Schwab, Tobias M. Kohl, Susanne Schnittger, Sabine Eichenlaub, Joachim W. Ellwart, Wolfgang Hiddemann, Karsten Spiekermann

Blood (2004) 103 (6): 2266–2275.

https://doi.org/10.1182/blood-2003-05-1653

Published: 2004

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Allorestricted T cells with specificity for the FMNL1-derived peptide PP2 have potent antitumor activity against hematologic and other malignancies

Point mutations in the juxtamembrane domain of FLT3 define a new class of activating mutations in AML

Point Mutations Found in the Juxtamembrane Domain of FLT3 Define a New Class of Activating Mutations in AML.

FLT3-ITD-TKD dual mutants associated with AML confer resistance to FLT3 PTK inhibitors and cytotoxic agents by overexpression of Bcl-x(L)

KIT exon 8 mutations associated with core-binding factor (CBF)–acute myeloid leukemia (AML) cause hyperactivation of the receptor in response to stem cell factor

Mutations in the tyrosine kinase domain of FLT3 define a new molecular mechanism of acquired drug resistance to PTK inhibitors in FLT3-ITD–transformed hematopoietic cells

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ASH Publications

American Society of Hematology

Update search

Allorestricted T cells with specificity for the FMNL1-derived peptide PP2 have potent antitumor activity against hematologic and other malignancies

Point mutations in the juxtamembrane domain of FLT3 define a new class of activating mutations in AML

Point Mutations Found in the Juxtamembrane Domain of FLT3 Define a New Class of Activating Mutations in AML.

FLT3-ITD-TKD dual mutants associated with AML confer resistance to FLT3 PTK inhibitors and cytotoxic agents by overexpression of Bcl-x(L)

KIT exon 8 mutations associated with core-binding factor (CBF)–acute myeloid leukemia (AML) cause hyperactivation of the receptor in response to stem cell factor

Mutations in the tyrosine kinase domain of FLT3 define a new molecular mechanism of acquired drug resistance to PTK inhibitors in FLT3-ITD–transformed hematopoietic cells

Email alerts

ASH Publications

American Society of Hematology

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